Treatments targeting inotropy
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Treatments targeting inotropy : A position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). / Maack, Christoph; Eschenhagen, Thomas; Hamdani, Nazha; Heinzel, Frank R.; Lyon, Alexander R.; Manstein, Dietmar; Metzger, Joseph; Papp, Zoltán; Tocchetti, Carlo G; Yilmaz, Mehmet Birhan; Anker, Stefan D.; Balligand, Jean-Luc; Bauersachs, Johann; Brutsaert, Dirk; Carrier, Lucie; Chlopicki, Stefan; Cleland, John G.; de Boer, Rudolf A.; Dietl, Alexander; Fischmeister, Rodolphe; Harjola, Veli-Pekka; Heymans, Stephane; Hilfiker-Kleiner, Denise; Holzmeister, Johannes; de Keulenaer, Gilles; Limongelli, Giuseppe; Linke, Wolfgang A; Lund, Lars H.; Masip, Josef; Metra, Marco; Mueller, Christian; Pieske, Burkert; Ponikowski, Piotr; Ristic, Arsen; Ruschitzka, Frank; Seferovic, Petar M.; Skouri, Hadi; Zimmermann, Wolfram H.; Mebazaa, Alexandre.
in: EUR HEART J, 2018.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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TY - JOUR
T1 - Treatments targeting inotropy
T2 - A position paper of the Committees on Translational Research and Acute Heart Failure of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)
AU - Maack, Christoph
AU - Eschenhagen, Thomas
AU - Hamdani, Nazha
AU - Heinzel, Frank R.
AU - Lyon, Alexander R.
AU - Manstein, Dietmar
AU - Metzger, Joseph
AU - Papp, Zoltán
AU - Tocchetti, Carlo G
AU - Yilmaz, Mehmet Birhan
AU - Anker, Stefan D.
AU - Balligand, Jean-Luc
AU - Bauersachs, Johann
AU - Brutsaert, Dirk
AU - Carrier, Lucie
AU - Chlopicki, Stefan
AU - Cleland, John G.
AU - de Boer, Rudolf A.
AU - Dietl, Alexander
AU - Fischmeister, Rodolphe
AU - Harjola, Veli-Pekka
AU - Heymans, Stephane
AU - Hilfiker-Kleiner, Denise
AU - Holzmeister, Johannes
AU - de Keulenaer, Gilles
AU - Limongelli, Giuseppe
AU - Linke, Wolfgang A
AU - Lund, Lars H.
AU - Masip, Josef
AU - Metra, Marco
AU - Mueller, Christian
AU - Pieske, Burkert
AU - Ponikowski, Piotr
AU - Ristic, Arsen
AU - Ruschitzka, Frank
AU - Seferovic, Petar M.
AU - Skouri, Hadi
AU - Zimmermann, Wolfram H.
AU - Mebazaa, Alexandre
PY - 2018
Y1 - 2018
N2 - Acute heart failure and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trialssuggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, phase II clinical trials suggest a favorable hemodynamic profile in patients with acute and chronic heart failure, and a phase III morbidity/mortality trial in patients with chronic heart failure has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with heart failure and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation-contraction coupling, we also discuss the impactof inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer term.
AB - Acute heart failure and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trialssuggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, phase II clinical trials suggest a favorable hemodynamic profile in patients with acute and chronic heart failure, and a phase III morbidity/mortality trial in patients with chronic heart failure has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with heart failure and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation-contraction coupling, we also discuss the impactof inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer term.
U2 - 10.1093/eurheartj/ehy600
DO - 10.1093/eurheartj/ehy600
M3 - SCORING: Review article
JO - EUR HEART J
JF - EUR HEART J
SN - 0195-668X
ER -